Objective:To explore the characteristics of attention bias and the role of embodied emotion prim-ing in college students with different traits of anxiety.Methods:From 2 310 college students,28 from low trait anxi-ety group and 30 from high trait anxiety group were selected based on the scores of the Trait Anxiety Scale.The at-tention bias index,attention orientation index and attention detachment difficulty index were calculated by point de-tection experiment.By asking two groups of subjects to change their body posture to induce embodied emotion,and then responding to the location of the detection point,the effects of embodied emotion priming on the attention bias of college students with different traits of anxiety were investigated.Results:The point detection experiment found that the attention detachment difficulty index of negative emotional faces in the high trait anxiety group was signifi-cantly greater than 0,and the attention orientation index of positive emotional faces in the low trait anxiety group was significantly greater than 0(Ps＜0.05).The attention bias index for positive emotional faces in low trait anxie-ty group was significantly higher than that in high trait anxiety group(P＜0.05).Under embodied negative prim-ing,the attention bias index of negative emotional faces in low trait anxiety group was significantly greater than 0(P＜0.05).The attention orientation indices of negative emotional faces were significantly higher than that of posi-tive emotional faces in both groups(P＜0.05).Conclusion:College students with high trait anxiety have difficulty in escaping attention to negative faces,while those with low trait anxiety have accelerated attention orientation to positive emotional faces.Embodied negative priming may have a greater impact onattention bias of towards negative emotional faces in students with low trait anxiety.

Objective:To explore the characteristics of attention bias and the role of embodied emotion prim-ing in college students with different traits of anxiety.Methods:From 2 310 college students,28 from low trait anxi-ety group and 30 from high trait anxiety group were selected based on the scores of the Trait Anxiety Scale.The at-tention bias index,attention orientation index and attention detachment difficulty index were calculated by point de-tection experiment.By asking two groups of subjects to change their body posture to induce embodied emotion,and then responding to the location of the detection point,the effects of embodied emotion priming on the attention bias of college students with different traits of anxiety were investigated.Results:The point detection experiment found that the attention detachment difficulty index of negative emotional faces in the high trait anxiety group was signifi-cantly greater than 0,and the attention orientation index of positive emotional faces in the low trait anxiety group was significantly greater than 0(Ps＜0.05).The attention bias index for positive emotional faces in low trait anxie-ty group was significantly higher than that in high trait anxiety group(P＜0.05).Under embodied negative prim-ing,the attention bias index of negative emotional faces in low trait anxiety group was significantly greater than 0(P＜0.05).The attention orientation indices of negative emotional faces were significantly higher than that of posi-tive emotional faces in both groups(P＜0.05).Conclusion:College students with high trait anxiety have difficulty in escaping attention to negative faces,while those with low trait anxiety have accelerated attention orientation to positive emotional faces.Embodied negative priming may have a greater impact onattention bias of towards negative emotional faces in students with low trait anxiety.

Objective:To find the chromosomal malfomations among microtia patients and the neighbouring genes of chromosomal aberrations or genes in the extra or deleted chromosome fragments would be screened to investigate the possible causative genes.Methods:According to the inclusion criteria, case group was selected from microtia patients referred to Plastic Surgery Hospital, Chinese Academy of Medical Science, between January 2012 and January 2014, and the control group was the normal people of similar age received plastic surgery in the same hospital in the same time who did not have any congenital genetic disease. Blood samples of two groups were collected, and genomic DNA was extracted, then copy number variation (CNV) analysis was performed in the two groups with gene chip technology and associated software for large fragment chromosomal malformations. The variations of chromosome copy number were recorded to further analyze the type and length of chromosome structure variation. The genes at the loci of break points were further screened referring to B allele frequency to interpret associated genes related to the occurrence of microtia. Fisher exact test were used for statistical analysis, and the difference was statistically significant ( P< 0.05). Results:942 patients with congenital microtia were included in the case group, 695 males and 247 females, aged (11.4±3.2) years; 1 802 normal controls, 1 290 males and 512 females, aged (11.6±4.9) years. Large chromosomal fragments variations were detected in 5 patients in chromosome in case group( P=0.003). The difference between the two groups was statistically significant( P=0.003). Three cases were found to carry an extra X chromosome. Among the 3 cases, one patient suffered from XXY karyotype and the other 2 patients X trisomy. Two cases were proved to be associated with chromosome structural variations. The malformations of the first case presented partial duplication of the long arm of chromosome 13 and 14. On searching for causative genes, OTX2, BMP4 and GSC were detected to be in the chromosome structural variations. The second case presented to be partial duplication of the long arm of chromosome 5. FGF pathway associated genes FGF18, FGFR4, FGF1 and BMP pathway associated genes FST, MSX2, SMAD5 were incorporated in the extra duplicated chromosome for possible gene dosage effect. Conclusions:The results indicated the possible association of chromosome abnormity and microtia and provide new insights in microtia-associated chromosome instability. Ten related genes were involved in the occurrence of microtia through various ways.

Objective:To find the chromosomal malfomations among microtia patients and the neighbouring genes of chromosomal aberrations or genes in the extra or deleted chromosome fragments would be screened to investigate the possible causative genes.Methods:According to the inclusion criteria, case group was selected from microtia patients referred to Plastic Surgery Hospital, Chinese Academy of Medical Science, between January 2012 and January 2014, and the control group was the normal people of similar age received plastic surgery in the same hospital in the same time who did not have any congenital genetic disease. Blood samples of two groups were collected, and genomic DNA was extracted, then copy number variation (CNV) analysis was performed in the two groups with gene chip technology and associated software for large fragment chromosomal malformations. The variations of chromosome copy number were recorded to further analyze the type and length of chromosome structure variation. The genes at the loci of break points were further screened referring to B allele frequency to interpret associated genes related to the occurrence of microtia. Fisher exact test were used for statistical analysis, and the difference was statistically significant ( P< 0.05). Results:942 patients with congenital microtia were included in the case group, 695 males and 247 females, aged (11.4±3.2) years; 1 802 normal controls, 1 290 males and 512 females, aged (11.6±4.9) years. Large chromosomal fragments variations were detected in 5 patients in chromosome in case group( P=0.003). The difference between the two groups was statistically significant( P=0.003). Three cases were found to carry an extra X chromosome. Among the 3 cases, one patient suffered from XXY karyotype and the other 2 patients X trisomy. Two cases were proved to be associated with chromosome structural variations. The malformations of the first case presented partial duplication of the long arm of chromosome 13 and 14. On searching for causative genes, OTX2, BMP4 and GSC were detected to be in the chromosome structural variations. The second case presented to be partial duplication of the long arm of chromosome 5. FGF pathway associated genes FGF18, FGFR4, FGF1 and BMP pathway associated genes FST, MSX2, SMAD5 were incorporated in the extra duplicated chromosome for possible gene dosage effect. Conclusions:The results indicated the possible association of chromosome abnormity and microtia and provide new insights in microtia-associated chromosome instability. Ten related genes were involved in the occurrence of microtia through various ways.

Objective To explore the therapeutic mechanism of kidney-reinforcing,blood-activating and phlegmresolving therapy for left ventricular fibrosis of spontaneously hypertensive rats (SHR).Methods Twenty SHR were randomly assigned to Chinese medicine group and model group.Additionally,ten Wistar-Kyoto(WKY) rats served as normal control group.After 12-week prevention,Masson staining method was used to measure the degree of fibrosis of left ventricular myocardial tissues,reverse transcription-polymerase chain reaction(RT-PCR) was used to detect Smad3 mRNA expression,and Western blotting method was used for the detection of Smad3 protein expression.Results The degree of left ventricular fibrosis myocardial tissue in Chinese medicine group was milder than that in the model group,and Samd3 protein and mRNA expression levels in Chinese medicine group were lower than those in the model group (P ＜ 0.05).Conclusion Kidney-reinforcing,blood-activating and phlegmresolving therapy can improve left ventricular fibrosis in SHR by inhibiting Smad3 expression.

Peripheral neuropathy( CIPN)induced by chemotherapy is the common dose-limiting adverse reactions of platinum,taxol and vinblastine. The mechanisms of CIPN due to platinum,taxol and vinblastine may be related to injury of dorsal root ganglion,inhibition of tubulin depolymerization and changing axonal transport,inhibition of association of tubulin from protein subunit,deletion of tubulin and dysfunction of axonal transport,respectively. Pain,numbness,acanthesthesia,burning sensation,sensory deprivation,myodynamia weakness or paralysation,constipation,sexual dysfunction,change of vision,and anaudia are the main clinical manifestations of CIPN. Usually,the amplitude and the conduction velocity of sensory nerve action potential are decreased,while the amplitude and the conduction velocity of motor nerve are normal or slightly changed before the clinical symptoms of CIPN appearance. The development of CIPN are related with sex( female),age( agedness),habits and customs( smoking history),tumor type (oophoroma),primary disease and combination with neurotoxic drug. The more the chemotherapeutics accumulated dose is, the higher the incidence of CIPN. The shorter the administration interval of chemotherapy is,the higher the incidence of CIPN. There is no effective drug for prevention of CIPN at present. Duloxetine is the the only one drug recommended by American Society of Clinical Oncology for treatment of CIPN.

Peripheral neuropathy( CIPN)induced by chemotherapy is the common dose-limiting adverse reactions of platinum,taxol and vinblastine. The mechanisms of CIPN due to platinum,taxol and vinblastine may be related to injury of dorsal root ganglion,inhibition of tubulin depolymerization and changing axonal transport,inhibition of association of tubulin from protein subunit,deletion of tubulin and dysfunction of axonal transport,respectively. Pain,numbness,acanthesthesia,burning sensation,sensory deprivation,myodynamia weakness or paralysation,constipation,sexual dysfunction,change of vision,and anaudia are the main clinical manifestations of CIPN. Usually,the amplitude and the conduction velocity of sensory nerve action potential are decreased,while the amplitude and the conduction velocity of motor nerve are normal or slightly changed before the clinical symptoms of CIPN appearance. The development of CIPN are related with sex( female),age( agedness),habits and customs( smoking history),tumor type (oophoroma),primary disease and combination with neurotoxic drug. The more the chemotherapeutics accumulated dose is, the higher the incidence of CIPN. The shorter the administration interval of chemotherapy is,the higher the incidence of CIPN. There is no effective drug for prevention of CIPN at present. Duloxetine is the the only one drug recommended by American Society of Clinical Oncology for treatment of CIPN.